Limits...
TyrR, the regulator of aromatic amino acid metabolism, is required for mice infection of Yersinia pestis.

Deng Z, Liu Z, He J, Wang J, Yan Y, Wang X, Cui Y, Bi Y, Du Z, Song Y, Yang R, Han Y - Front Microbiol (2015)

Bottom Line: Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene.Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions.In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli.

View Article: PubMed Central - PubMed

Affiliation: Department of Sanitary Inspection, School of Public Health, University of South China Hengyang, China ; State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology Beijing, China.

ABSTRACT
Yersinia pestis, the causative agent of plague, poses a serious health threat to rodents and human beings. TyrR is a transcriptional regulator (TyrR) that controls the metabolism of aromatic amino acids in Escherichia coli. In this paper, TyrR played an important role in Y. pestis virulence. Inactivation of tyrR did not seem to affect the in vitro growth of this organism, but resulted in at least 10,000-fold attenuation compared with the wild-type (WT) strain upon subcutaneous infection to mice. In addition, loads of tyrR mutant within mice livers and spleens significantly decreased compared with the WT strain. Transcriptome analysis revealed that TyrR, directly or indirectly, regulated 29 genes encoded on Y. pestis chromosome or plasmids under in vitro growth condition. Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene. Two genes (glnL and glnG) that encode sensory histidine kinase and regulator in a two-component regulatory system involved in nitrogen assimilation were downregulated in the tyrR mutant. Several genes encoding type III secretion proteins were transcribed by 2.0-4.2-fold in a tyrR mutant relative to the WT strain. Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions. In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli. TyrR is a metabolic virulence determinant in Y. pestis that is important for extracellular survival and/or proliferation.

No MeSH data available.


Related in: MedlinePlus

Transcription measurements of eight genes were chosen for quantitative RT-PCR validation. The real-time PCR log2 values were plotted against the RNA-seq data log2 values. The coefficient of determination (R2) for comparison of the two datasets is 0.991.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4325908&req=5

Figure 4: Transcription measurements of eight genes were chosen for quantitative RT-PCR validation. The real-time PCR log2 values were plotted against the RNA-seq data log2 values. The coefficient of determination (R2) for comparison of the two datasets is 0.991.

Mentions: Eight genes were selected for qPCR analysis to validate the RNA-seq data. A high correlation (R2 = 0.988) was observed between expression values obtained by RNA-seq and qPCR (Figure 4). Aromatic-pathway genes were confirmed to be regulated by TyrR in E. coli (Pittard et al., 2005). As expected, the aroF-tyrA operon responsible for aromatic biosynthesis and aroL, aroP and tyrP for aromatic transport were most strongly upregulated. Two genes responsible for acid stress, hdeB and hdeD, were confirmed to be downregulated upon deletion of tyrR gene, and this finding was consistent with the observation on the compromised tolerance to acid stress in in vitro assays (Figure 1).


TyrR, the regulator of aromatic amino acid metabolism, is required for mice infection of Yersinia pestis.

Deng Z, Liu Z, He J, Wang J, Yan Y, Wang X, Cui Y, Bi Y, Du Z, Song Y, Yang R, Han Y - Front Microbiol (2015)

Transcription measurements of eight genes were chosen for quantitative RT-PCR validation. The real-time PCR log2 values were plotted against the RNA-seq data log2 values. The coefficient of determination (R2) for comparison of the two datasets is 0.991.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4325908&req=5

Figure 4: Transcription measurements of eight genes were chosen for quantitative RT-PCR validation. The real-time PCR log2 values were plotted against the RNA-seq data log2 values. The coefficient of determination (R2) for comparison of the two datasets is 0.991.
Mentions: Eight genes were selected for qPCR analysis to validate the RNA-seq data. A high correlation (R2 = 0.988) was observed between expression values obtained by RNA-seq and qPCR (Figure 4). Aromatic-pathway genes were confirmed to be regulated by TyrR in E. coli (Pittard et al., 2005). As expected, the aroF-tyrA operon responsible for aromatic biosynthesis and aroL, aroP and tyrP for aromatic transport were most strongly upregulated. Two genes responsible for acid stress, hdeB and hdeD, were confirmed to be downregulated upon deletion of tyrR gene, and this finding was consistent with the observation on the compromised tolerance to acid stress in in vitro assays (Figure 1).

Bottom Line: Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene.Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions.In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli.

View Article: PubMed Central - PubMed

Affiliation: Department of Sanitary Inspection, School of Public Health, University of South China Hengyang, China ; State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology Beijing, China.

ABSTRACT
Yersinia pestis, the causative agent of plague, poses a serious health threat to rodents and human beings. TyrR is a transcriptional regulator (TyrR) that controls the metabolism of aromatic amino acids in Escherichia coli. In this paper, TyrR played an important role in Y. pestis virulence. Inactivation of tyrR did not seem to affect the in vitro growth of this organism, but resulted in at least 10,000-fold attenuation compared with the wild-type (WT) strain upon subcutaneous infection to mice. In addition, loads of tyrR mutant within mice livers and spleens significantly decreased compared with the WT strain. Transcriptome analysis revealed that TyrR, directly or indirectly, regulated 29 genes encoded on Y. pestis chromosome or plasmids under in vitro growth condition. Similar to the regulatory function of this protein in E. coli, five aromatic-pathway genes (aroF-tyrA, aroP, aroL, and tyrP) were significantly reduced upon deletion of the tyrR gene. Two genes (glnL and glnG) that encode sensory histidine kinase and regulator in a two-component regulatory system involved in nitrogen assimilation were downregulated in the tyrR mutant. Several genes encoding type III secretion proteins were transcribed by 2.0-4.2-fold in a tyrR mutant relative to the WT strain. Interestingly, the acid-stressed genes, hdeB and hdeD, were downregulated, and such downregulation partly accounted for the decrease in tolerance of the tyrR mutant under acidic conditions. In conclusion, regulation of TyrR in Y. pestis is similar to, but distinct from, that in E. coli. TyrR is a metabolic virulence determinant in Y. pestis that is important for extracellular survival and/or proliferation.

No MeSH data available.


Related in: MedlinePlus